Recovery of function after lesions in the superior temporal sulcus in the monkey

1991 ◽  
Vol 66 (3) ◽  
pp. 651-673 ◽  
Author(s):  
D. S. Yamasaki ◽  
R. H. Wurtz
Keyword(s):  
Smooth Pursuit ◽  
Visual Motion ◽  
Visual Fields ◽  
Ibotenic Acid ◽  
Superior Temporal Sulcus ◽  
Position Error ◽  
Eye Position ◽  
Motion Information ◽  
Temporal Area ◽  
Rate Of Recovery

1. Ibotenic acid lesions in the monkey's middle temporal area (MT) and the medial superior temporal area (MST) in the superior temporal sulcus (STS) have previously been shown to produce a deficit in initiation of smooth-pursuit eye movements to moving visual targets. The deficits, however, recovery within a few days. In the present experiments we investigated the factors that influence that recovery. 2. We tested two aspects of the monkey's ability to use motion information to acquire moving targets. We used eye-position error as a measure of the monkey's ability to make accurate initial saccades to the moving target. We measured eye speed within the first 100 ms after the saccade to evaluate the monkey's initial smooth pursuit. 3. We determined that pursuit recovery was not dependent specifically on the use of neurotoxic lesions. Although the rate of recovery was slightly altered by replacing the usual neurotoxin (ibotenic acid) with another neurotoxin [alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)] or with an electrolytic lesion, pursuit recovery still occurred within a period of days to weeks. 4. There was a relationship between the size and location of the lesion and the recovery time. The time to recovery for eye-position error and initial eye speed increased with the fraction of MT removed. Whether the rate of recovery and size of lesions within regions on the anterior bank were related was unresolved. 5. We found that a large AMPA lesion within the STS that removed all of MT and nearly all of MST drastically altered the rate of recovery. Recovery was incomplete more than 7 mo after the lesion. Even with this lesion, however, the monkey's ability to use motion information for pursuit was not completely eliminated. 6. The large lesion also included parts of areas V1, V2, V3, and V4, but analysis of the visual fields associated with this lesion indicated that these areas probably did not have a substantial effect on recovery. 7. We tested whether visual motion experience of the monkey after a lesion was necessary for recovery by limiting the monkey's experience either by using a mask or by using 4-Hz stroboscopic illumination. In one monkey the eye-position error component of pursuit was prolonged to greater than 2 wk, but recovery of eye speed was not. Reduced motion experience had little effect on recovery in the other two monkeys. These results suggest that such visual motion experience is not necessary for the recovery of pursuit.(ABSTRACT TRUNCATED AT 400 WORDS)

Pursuit and optokinetic deficits following chemical lesions of cortical areas MT and MST

1988 ◽  
Vol 60 (3) ◽  
pp. 940-965 ◽  
Author(s):  
M. R. Dursteler ◽  
R. H. Wurtz
Keyword(s):  
Eye Movements ◽  
Visual Field ◽  
Visual Motion ◽  
Ibotenic Acid ◽  
Motion Processing ◽  
Temporal Area ◽  
Target Speed ◽  
Pursuit Eye Movements ◽  
Medial Superior Temporal ◽  
Visual Motion Processing

1. Previous experiments have shown that punctate chemical lesions within the middle temporal area (MT) of the superior temporal sulcus (STS) produce deficits in the initiation and maintenance of pursuit eye movements (10, 34). The present experiments were designed to test the effect of such chemical lesions in an area within the STS to which MT projects, the medial superior temporal area (MST). 2. We injected ibotenic acid into localized regions of MST, and we observed two deficits in pursuit eye movements, a retinotopic deficit and a directional deficit. 3. The retinotopic deficit in pursuit initiation was characterized by the monkey's inability to match eye speed to target speed or to adjust the amplitude of the saccade made to acquire the target to compensate for target motion. This deficit was related to the initiation of pursuit to targets moving in any direction in the visual field contralateral to the side of the brain with the lesion. This deficit was similar to the deficit we found following damage to extrafoveal MT except that the affected area of the visual field frequently extended throughout the entire contralateral visual field tested. 4. The directional deficit in pursuit maintenance was characterized by a failure to match eye speed to target speed once the fovea had been brought near the moving target. This deficit occurred only when the target was moving toward the side of the lesion, regardless of whether the target began to move in the ipsilateral or contralateral visual field. There was no deficit in the amplitude of saccades made to acquire the target, or in the amplitude of the catch-up saccades made to compensate for the slowed pursuit. The directional deficit is similar to the one we described previously following chemical lesions of the foveal representation in the STS. 5. Retinotopic deficits resulted from any of our injections in MST. Directional deficits resulted from lesions limited to subregions within MST, particularly lesions that invaded the floor of the STS and the posterior bank of the STS just lateral to MT. Extensive damage to the densely myelinated area of the anterior bank or to the posterior parietal area on the dorsal lip of the anterior bank produced minimal directional deficits. 6. We conclude that damage to visual motion processing in MST underlies the retinotopic pursuit deficit just as it does in MT. MST appears to be a sequential step in visual motion processing that occurs before all of the visual motion information is transmitted to the brainstem areas related to pursuit.(ABSTRACT TRUNCATED AT 400 WORDS)

MST Neuronal Responses to Heading Direction During Pursuit Eye Movements

1999 ◽  
Vol 81 (2) ◽  
pp. 596-610 ◽  
Author(s):  
William K. Page ◽  
Charles J. Duffy
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Visual Motion ◽  
Neuronal Population ◽  
Smooth Pursuit Eye Movements ◽  
Neuronal Responses ◽  
Temporal Area ◽  
Pursuit Eye Movements ◽  
Heading Direction ◽  
Monkey Visual Cortex

MST neuronal responses to heading direction during pursuit eye movements. As you move through the environment, you see a radial pattern of visual motion with a focus of expansion (FOE) that indicates your heading direction. When self-movement is combined with smooth pursuit eye movements, the turning of the eye distorts the retinal image of the FOE but somehow you still can perceive heading. We studied neurons in the medial superior temporal area (MST) of monkey visual cortex, recording responses to FOE stimuli presented during fixation and smooth pursuit eye movements. Almost all neurons showed significant changes in their FOE selective responses during pursuit eye movements. However, the vector average of all the neuronal responses indicated the direction of the FOE during both fixation and pursuit. Furthermore, the amplitude of the net vector increased with increasing FOE eccentricity. We conclude that neuronal population encoding in MST might contribute to pursuit-tolerant heading perception.

Horizontal Smooth Pursuit Adaptation in Macaques After Muscimol Inactivation of the Dorsolateral Pontine Nucleus (DLPN)

2007 ◽  
Vol 98 (5) ◽  
pp. 2918-2932 ◽  
Author(s):  
Seiji Ono ◽  
Michael J. Mustari
Keyword(s):  
Smooth Pursuit ◽  
Visual Motion ◽  
T Test ◽  
Motion Information ◽  
Unit Recording ◽  
Pontine Nucleus ◽  
Dorsolateral Pontine Nucleus ◽  
Step Down ◽  
Ventral Paraflocculus

The smooth pursuit (SP) system can adapt its response to developmental changes, injury, and behavioral context. Previous lesion and single-unit recording studies show that the macaque cerebellum plays a role in SP initiation, maintenance, and adaptation. The aim of this study was to determine the potential role of the DLPN in SP adaptation. The DLPN receives inputs from the cortical SP system and delivers eye and visual motion information to the dorsal/ventral paraflocculus and vermis of the cerebellum. We studied SP adaptation in two juvenile rhesus monkeys ( Macaca mulatta), using double steps of target speed that step- up (10–30°/s) or step-down (25–5°/s). We used microinjection of muscimol (≤2%; 0.15 μl) to reversibly inactivate the DLPN, unilaterally. After DLPN inactivation, initial ipsilesional SP acceleration (first 100 ms) was significantly reduced by 47–74% ( P < 0.01; unpaired t-test) of control values in the single-speed step-ramp paradigm. Similarly, ipsilesional steady-state SP velocity was also reduced by 59–78% ( P < 0.01; unpaired t-test) of control values. Contralesional SP was not impaired after DLPN inactivation. Control testing showed significant adaptive changes of initial SP eye acceleration after 100 trials in either step-up or step-down paradigms. After inactivation, during ipsilesional SP, adaptation was impaired in the step-up but not in the step-down paradigm. In contrast, during contralesional tracking, adaptive capability remained in the step-down but not in the step-up paradigm. Therefore SP adaptation could depend, in part, on direction sensitive eye/visual motion information provided by DLPN neurons to cerebellum.

scholarly journals Response properties of MST parafoveal neurons during smooth pursuit adaptation

2016 ◽  
Vol 116 (1) ◽  
pp. 210-217 ◽  
Author(s):  
Seiji Ono ◽  
Michael J. Mustari
Keyword(s):  
Smooth Pursuit ◽  
Time Course ◽  
Visual Motion ◽  
Visual Stimulation ◽  
Critical Role ◽  
Visual Sensitivity ◽  
Large Field ◽  
Target Velocity ◽  
Visual Response ◽  
Temporal Area

Visual motion neurons in the posterior parietal cortex play a critical role in the guidance of smooth pursuit eye movements. Initial pursuit (open-loop period) is driven, in part, by visual motion signals from cortical areas, such as the medial superior temporal area (MST). The purpose of this study was to determine whether adaptation of initial pursuit gain arises because of altered visual sensitivity of neurons at the cortical level. It is well known that the visual motion response in MST is suppressed after exposure to a large-field visual motion stimulus, showing visual motion adaptation. One hypothesis is that foveal motion responses in MST are associated with smooth pursuit adaptation using a small target spot. We used a step-ramp tracking task with two steps of target velocity (double-step paradigm), which induces gain-down or gain-up adaptation. We found that after gain-down adaptation 58% of our MST visual neurons showed a significant decrease in firing rate. This was the case even though visual motion input (before the pursuit onset) from target motion was constant. Therefore, repetitive visual stimulation during the gain-down paradigm could lead to adaptive changes in the visual response. However, the time course of adaptation did not show a correlation between the visual response and pursuit behavior. These results indicate that the visual response in MST may not directly contribute to the adaptive change in pursuit initiation.

Relation of cortical areas MT and MST to pursuit eye movements. I. Localization and visual properties of neurons

1988 ◽  
Vol 60 (2) ◽  
pp. 580-603 ◽  
Author(s):  
H. Komatsu ◽  
R. H. Wurtz
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Visual Motion ◽  
Receptive Fields ◽  
Motion Processing ◽  
Temporal Area ◽  
Pursuit Eye Movements ◽  
Visual Motion Processing ◽  
Visual Areas ◽  
Visual Properties

1. Among the multiple extrastriate visual areas in monkey cerebral cortex, several areas within the superior temporal sulcus (STS) are selectively related to visual motion processing. In this series of experiments we have attempted to relate this visual motion processing at a neuronal level to a behavior that is dependent on such processing, the generation of smooth-pursuit eye movements. 2. We studied two visual areas within the STS, the middle temporal area (MT) and the medial superior temporal area (MST). For the purposes of this study, MT and MST were defined functionally as those areas within the STS having a high proportion of directionally selective neurons. MST was distinguished from MT by using the established relationship of receptive-field size to eccentricity, with MST having larger receptive fields than MT. 3. A subset of these visually responsive cells within the STS were identified as pursuit cells--those cells that discharge during smooth pursuit of a small target in an otherwise dark room. Pursuit cells were found only in localized regions--in the foveal region of MT (MTf), in a dorsal-medial area of MST on the anterior bank of the STS (MSTd), and in a lateral-anterior area of MST on the floor and the posterior bank of the STS (MST1). 4. Pursuit cells showed two characteristics in common when their visual properties were studied while the monkey was fixating. Almost all cells showed direction selectivity for moving stimuli and included the fovea within their receptive fields. 5. The visual response of pursuit cells in the several areas differed in two ways. Cells in MTf preferred small moving spots of light, whereas cells in MSTd preferred large moving stimuli, such as a pattern of random dots. Cells in MTf had small receptive fields; those in MSTd usually had large receptive fields. Visual responses of pursuit neurons in MST1 were heterogeneous; some resembled those in MTf, whereas others were similar to those in MSTd. This suggests that the pursuit cells in MSTd and MST1 belong to different subregions of MST.

Smooth-pursuit eye movement deficits with chemical lesions in the dorsolateral pontine nucleus of the monkey

1988 ◽  
Vol 59 (3) ◽  
pp. 952-977 ◽  
Author(s):  
J. G. May ◽  
E. L. Keller ◽  
D. A. Suzuki
Keyword(s):  
Steady State ◽  
Eye Movements ◽  
Smooth Pursuit ◽  
Visual Motion ◽  
Ibotenic Acid ◽  
Smooth Pursuit Eye Movements ◽  
Optokinetic Response ◽  
Pontine Nucleus ◽  
Pursuit Eye Movements ◽  
Dorsolateral Pontine Nucleus

1. Anatomical and single-unit recording studies suggest that the dorsolateral pontine nucleus (DLPN) in monkey is a major link in the projection of descending visual motion information to the cerebellum. Such studies coupled with cortical and cerebellar lesion results suggest a major role for this basilar pontine region in the mediation of smooth-pursuit eye movements. 2. To provide more direct evidence that this pontine region is involved in the control of smooth-pursuit eye movements, focal chemical lesions were made in DLPN in the vicinity of previously recorded visual motion and pursuit-related neurons. Eye movement responses were subsequently recorded in these lesioned animals under several behavioral paradigms. 3. A major deficit in smooth-pursuit performance was produced after unilateral DLPN lesions generated either reversibly with lidocaine or more permanently with ibotenic acid. Pursuit impairments were observed during steady-state tracking of sinusoidal target motion as well as during the initiation of pursuit tracking to sudden ramp target motion. Through the use of the latter technique, initial eye acceleration was reduced to less than one-half of normal for animals with large lesions of the dorsolateral and lateral pontine nuclei. 4. The pursuit deficit in all animals was directional in nature and was not dependent on the visual hemifield in which the motion stimulus occurred. The largest effect for horizontal tracking occurred in all animals for pursuit directed ipsilateral to the lesion. Animals also showed major deficits in one or both directions of vertical pursuit, although the primary direction of the vertical impairment was variable from animal to animal. 5. Chemical lesions in the DLPN also produced comparable deficits in the initiation of optokinetic-induced smooth eye movements in the ipsilateral direction. In contrast to this effect on the initial optokinetic response, in the one lesioned animal studied during prolonged constant velocity optokinetic drum rotation, smooth eye speed increased slowly over a 10- to 15-s period to reach a level that closely matched drum speed. These results suggest that pathways outside the DLPN can generate the steady-state optokinetic response. 6. Saccades to stationary targets were normal after DLPN lesions, but corrective saccades made to targets moving in the direction ipsilateral to the lesion were much more hypometric than similar prelesion control saccades. 7. The pursuit deficits produced by lidocaine injections recovered within 30 min. The ibotenic acid deficits were maximal approximately 1 day after the injection and recovered rapidly thereafter over a time period of 3-7 days.(ABSTRACT TRUNCATED AT 400 WORDS)

Oculomotor biomarkers of illness, risk, and pharmacogenetic treatment effects across the psychosis spectrum

2020 ◽  
pp. 234-244
Author(s):  
James L. Reilly ◽  
Jennifer McDowell ◽  
Jeffrey Bishop ◽  
Andreas Sprenger ◽  
Rebekka Lencer
Keyword(s):  
Eye Movement ◽  
Smooth Pursuit ◽  
Visual Motion ◽  
Gene Variants ◽  
Motion Information ◽  
Antisaccade Task ◽  
Movement Performance ◽  
Research Findings ◽  
Sensorimotor Processes ◽  
Psychotic Bipolar Disorder

Eye movements are used to assess alterations in brain systems involved in cognitive and sensorimotor processes in psychiatric disorders. This chapter summarizes findings comparing saccadic and smooth pursuit eye movement performance across psychotic proband and relative groups, with an emphasis on schizophrenia, schizoaffective disorder, and psychotic bipolar disorder. Inhibitory errors on the antisaccade task represent a robust and graded deficit across probands, with greatest impairment observed in schizophrenia, and among relatives, particularly those with elevated psychosis spectrum traits. Abnormalities in the use of early visual motion information during smooth pursuit is apparent among both probands and relatives, while deficient use of visual feedback for dynamical pursuit appears restricted to probands. Select eye movement measures appear differentially affected by glutamate and dopamine gene variants. Overall, research findings support eye movement measures as promising biomarkers of altered brain systems underlying select cognitive and sensorimotor processes across the psychosis spectrum.

Directional pursuit deficits following lesions of the foveal representation within the superior temporal sulcus of the macaque monkey

1987 ◽  
Vol 57 (5) ◽  
pp. 1262-1287 ◽  
Author(s):  
M. R. Dursteler ◽  
R. H. Wurtz ◽  
W. T. Newsome
Keyword(s):  
Visual Field ◽  
Visual Motion ◽  
Ibotenic Acid ◽  
Macaque Monkey ◽  
Superior Temporal Sulcus ◽  
Target Motion ◽  
Motion Processing ◽  
Position Information ◽  
Field Representation ◽  
Visual Motion Processing

Ibotenic acid lesions of the middle temporal visual area (MT) have previously been shown to impair a monkey's ability to initiate smooth pursuit eye movements to targets moving in the extrafoveal visual field (30). This is a retinotopic deficit: pursuit is impaired in all directions within the affected portion of the contralateral visual field. In the present experiments we analyzed the effects of lesions of the foveal representation of MT on the maintenance of foveal pursuit. Injections of ibotenic acid were directed toward the representation of the fovea within MT but spread into extrafoveal regions of MT and adjacent visual areas within the superior temporal sulcus. Chemical lesions of the foveal representation produced a directional deficit in the maintenance of pursuit: the monkey failed to match eye speed to target speed when pursuing a target that moved toward the side of the brain with the lesion. This deficit was evident regardless of the part of the visual field in which target motion began, and pursuit at higher target speeds was more severely affected. The directional deficit was qualitatively similar to pursuit deficits observed in human patients following large parietal-occipital lesions. Extension of the lesions into extrafoveal regions of the contralateral visual field representation also resulted in retinotopic deficits for pursuit initiation: the monkey was unable to match the speed of its pursuit eye movement to that of a target or to adjust the amplitude of its saccade to compensate for target motion. The errors in pursuit speed and saccade amplitude for initiation of pursuit into the contralateral visual field were linearly related, which supports the hypothesis that both deficits arise from damage to the same underlying visual motion processing mechanism. The selectivity of the retinotopic deficit for motion information was also investigated by reducing retinal motion through the use of a stabilized image. After the lesion, the monkeys continued normal pursuit when a position error was present during stabilization, supporting the view that the deficit was related to loss of motion but not position information.

scholarly journals Eye Position Error Influence over “Open-Loop” Smooth Pursuit Initiation

2019 ◽  
Vol 39 (14) ◽  
pp. 2709-2721 ◽  
Author(s):  
Antimo Buonocore ◽  
Julianne Skinner ◽  
Ziad M. Hafed
Keyword(s):  
Smooth Pursuit ◽  
Open Loop ◽  
Position Error ◽  
Eye Position ◽  
Pursuit Initiation

Eye Movement Deficits Following Ibotenic Acid Lesions of the Nucleus Prepositus Hypoglossi in Monkeys II. Pursuit, Vestibular, and Optokinetic Responses

1999 ◽  
Vol 81 (2) ◽  
pp. 668-681 ◽  
Author(s):  
Chris R. S. Kaneko
Keyword(s):  
Eye Movements ◽  
Eye Movement ◽  
Smooth Pursuit ◽  
Ibotenic Acid ◽  
Eye Position ◽  
Neural Integrator ◽  
Nucleus Prepositus Hypoglossi ◽  
Optokinetic Responses ◽  
Prepositus Hypoglossi ◽  
Eye Velocity

Eye movement deficits following ibotenic acid lesions of the nucleus prepositus hypoglossi in monkeys. II. Pursuit, vestibular, and optokinetic responses. The eyes are moved by a combination of neural commands that code eye velocity and eye position. The eye position signal is supposed to be derived from velocity-coded command signals by mathematical integration via a single oculomotor neural integrator. For horizontal eye movements, the neural integrator is thought to reside in the rostral nucleus prepositus hypoglossi (nph) and project directly to the abducens nuclei. In a previous study, permanent, serial ibotenic acid lesions of the nph in three rhesus macaques compromised the neural integrator for fixation but saccades were not affected. In the present study, to determine further whether the nph is the neural substrate for a single oculomotor neural integrator, the effects of those lesions on smooth pursuit, the vestibulo-ocular reflex (VOR), vestibular nystagmus (VN), and optokinetic nystagmus (OKN) are documented. The lesions were correlated with long-lasting deficits in eye movements, indicated most clearly by the animals’ inability to maintain steady gaze in the dark. However, smooth pursuit and sinusoidal VOR in the dark, like the saccades in the previous study, were affected minimally. The gain of horizontal smooth pursuit (eye movement/target movement) decreased slightly (<25%) and phase lead increased slightly for all frequencies (0.3–1.0 Hz, ±10° target tracking), most noticeably for higher frequencies (0.8–0.7 and ∼20° for 1.0-Hz tracking). Vertical smooth pursuit was not affected significantly. Surprisingly, horizontal sinusoidal VOR gain and phase also were not affected significantly. Lesions had complex effects on both VN and OKN. The plateau of per- and postrotatory VN was shortened substantially (∼50%), whereas the initial response and the time constant of decay decreased slightly. The initial OKN response also decreased slightly, and the charging phase was prolonged transiently then recovered to below normal levels like the VN time constant. Maximum steady-state, slow eye velocity of OKN decreased progressively by ∼30% over the course of the lesions. These results support the previous conclusion that the oculomotor neural integrator is not a single neural entity and that the mathematical integrative function for different oculomotor subsystems is most likely distributed among a number of nuclei. They also show that the nph apparently is not involved in integrating smooth pursuit signals and that lesions of the nph can fractionate the VOR and nystagmic responses to adequate stimuli.

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